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The Corner: What You Know Might Hurt You!
By Bob Albright
11/11/2009 |
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Hyponatremia: “What you know may hurt you!”
Most endurance athletes know a few things about low serum sodium levels (hyponatremia). They know it’s common, they know it is caused by drinking too much water and they know that supplementing sodium will treat and/or prevent the problem. Hmm, well, what we “know” may hurt us.
Actually the incidence of documented hyponatremia among endurance athletes is extremely low. The clinical signs and symptoms attributed to hyponatremia are very diverse, and often (especially with respect to cramping) turn out to be unrelated as the measured sodium levels turn out to be normal. Presuming any unusual symptom we experience as we pursue our passion of endurance sports is due to hyponatremia may mask other more serious issues.
Many have laid the blame for hyponatremia at the feet of excess water ingestion, often along with inadequate sodium supplementation. While it is true that, as a group, the athletes diagnosed with hyponatremia tended to have ingested more water and were out on course longer, the direct causal link needs to be examined much more carefully.
The human body is a marvelous survival machine. Our species can thrive in deserts, rain forests and most anything in between. While much of our adaptation may be due to our ability to modify our immediate environment, I argue it’s because of our kidneys!
We have an incredible ability to maintain internal balance of blood chemistry. In fact our blood’s density (osmolality) varies by less than 0.01% under physiologic circumstances. Sodium is the principle agent which contributes over 96% of our serum’s density (osmolality). We very jealously guard our osmolality via receptors in the brainstem. These osmoreceptors will become stimulated if the osmolality rises even slightly. Think dehydration; a huge salt load; or enough sugar / fat. This will trigger the very powerful stimulus to DRINK. Ingestion of water (if it is absorbed—more on that later) will “dilute” the blood restoring balance. Additionally, the increase in osmolality also triggers the release of a compound known as vasopressin (anti-diuretic hormone- ADH) from the pituitary gland (brainstem). This compound instructs the kidneys to IMMEDIATELY begin maximum urinary concentration via conservation of water.
Vice versa is true as well. If our body’s sodium level decreases even slightly, the ADH will shut off and thirst is abolished. Our kidneys can excrete more than 13 liters per day of water without one single point change in the sodium level!
Whoa! So how in the world does an athlete drinking far less than 13 liters become hyponatremic?
Before we get to that, we need to remember my prior point that we are marvelous survival machines. We regulate the concentration of the bloodstream separately from maintaining adequate organ perfusion. Perhaps the major threat to our existence is low effective circulating volume in our blood vessels. The brainstem and major blood vessels have receptors which respond to low flow states and stimulate the body’s compensatory mechanisms to restore circulation. We maintain this “effective volume” by means of enhancing the cardiovascular system’s efficiency. This occurs via adaptations of heart rate, cardiac pumping volume and vessel tone (ie. opening or constricting of the vessel beds); and the interplay of, you guessed it, the kidneys!
Our kidneys sense delivery of blood flow. When the kidneys are under perfused, they react by triggering increase in blood pressure and sodium retention, thus restoring the normal situation. Vice versa, if we eat a tremendous load of salt—without the low volume issue—we simply excrete the salt! These effects are not guided by blood concentrations of sodium, but by whether or not we need to conserve or release sodium and hence fluid.
But isn’t there any cross over in the system?
A key point in the understanding of hyponatremia among athletes relates to the extremes of physiology which occcur. When effective circulating volume declines below a critical threshold (greater than 15 % decrease in volume—which could be due to SEVERE dehydration) stimulation of sodium resorption (via the kidneys), increases in heart rate, enhanced cardiac pumping function and blood vessel constriction occurs. However, the brainstem contributes an additional adaptation, which is a “good news/ bad news” situation. Severely compromised effective circulating volume triggers the release of vasopressin – ADH. This is explained by our need to restore the circulation via any means necessary in these dire situations. So, in order to persevere our life (good news) we become hyponatremic (bad news).
Athletes in this situation are very, very dehydrated. Their mucous membranes will be dry; they will have a fast heart rate; and, usually, low blood pressure. They will have lost significant weight from the start of the event.
When this situation occurs, restoration of the circulating volume is mandated ASAP! Usually intravenous saline (0.9%) is the fluid of choice. Once the circulation is restored, the stimulus for vasopressin-ADH release ceases, and the low sodium concentration is quickly corrected by the kidneys as they get rid of all the free water.
OK, so how does this happen to folks who are NOT depleted from an effective circulating volume perspective?
The answer lies in the release of vasopressin- ADH from a “non-osmolality” stimulus. Fear, pain, nausea, vomiting, shortness of breath (in general-- all significant physiologic stressors) are potent causes for release of vasopressin and ADH!
Medical professionals call this SIADH (syndrome of inappropriate antidiuretic hormone). To make maters worse, non-steroidal antiinflammatory drugs (NSAIDS) block water excretion hence- making the sodium concentration even lower. Additionally, certain medications such as the commonly-prescribed Selective Serotonin Reuptake inhibitors (SSRI drugs for depression) are well documented stimulators of vasopressin- ADH release!
The symptoms of confusion, vision changes, lethargy, weakness and headache are no less evident than among the athletes with VERY low volume but its cause and treatment are vastly different.
So, take one part anxious athlete, one part going a bit too hard (or too long), add pain, nausea and maybe too much water –like fluids on the course and viola! Hyponatremia.
This is by far the most common scenario seen at endurance events. The treatment for these type athletes is hypertonic (very dense, high osmolality, 3%) saline IV solutions. These solutions are required to “overwhelm” the kidney’s tendency to retain water, while using the kidney’s natural tendency to excrete the sodium load. The kidney does not need to save the sodium; given the absence of low effective circulating volume.
Drinking water alone does not cause this problem, nor can it simply be remedied by eating lots of sodium. An issue which is often ignored is the rate of absorption of both water and solutes (anything suspended in the water). During intense muscular exertion, blood flow is preferentially sent to the muscles. This leaves less for digestion and fluid/solute absorption. Therefore assuming ingestion of a certain amount of sodium or water will get taken into the circulation is an uncertain assumption at best.
What is the athlete to do?
1. Be as well trained for the upcoming event as possible.
2. Match your expectations (and pacing) to your training.
3. Be as acclimatized to the environment as possible.
4. When nausea, or other “digestion problems” occur, slow down, allow the gut to regain function.
5. Replace your sodium losses: note each liter of sweat has only 40-80 mg of sodium, at most. For most of us, 200-400 mg. sodium per hour is more than sufficient (assuming we are absorbing it).
6. Avoid severe dehydration (seems a no brainer—but see above) water only may be fine for shorter events (< 90 min. or so).
7. NO NSAIDS!
8. Caution - ask your physician about SSRI agents and endurance activities.
9. Weigh yourself prior to your event and write it down on you race number—this will help guide the medical personnel to give the correct therapy if you do develop hyponatremia
10. Get tested: If you have experienced serious hyponatremia (or think you have), it’s worthwhile to see a physician who may order an electrolyte (blood chemistry) screen during a race simulation workout. This can be facilitated by having a prescription written for the blood testing, which can be given to the lab personnel at the testing facility (often a lab at a hospital) at your convienience. If hyponatremia is confirmed, a more thorough evaluation is warranted. Your physician may even wish to check specific urine chemistries, as well as, serum adrenal and thyroid function testing.
I do need to emphasize, not all unusual symptoms we experience during our events are hyponatremia-related, and getting a cause and treatment sorted out is well worth it.
Now what you know won’t hurt you!
Bob Albright is a multiple Ironman-finisher and buddy of Gordo’s at Endurance Corner. When not attending to his duties as husband, father and triathlete… he can be found at the Mayo Clinic in Rochester, MN, where he works as an Assistant Professor of Medicine and as a Nephrologist (Kidney Doc).
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